Background: Breast cancer has been the first death cause of cancer in women all over the world. Metastasis is believed to be the most important process for treating breast cancer. There is evidence that lncRNA functions as a tumor suppressor in breast cancer metastasis. However, upstream regulation of in breast cancer remain elusive. Therefore, it is critical to elucidate the underlying mechanism upstream MEG3 to regulate breast cancer metastasis.
Methods: We employed RT-qPCR and Western blot to examine expression level of -, DNMT1, SP1, SP3 and . Besides, methylation-specific PCR was used to determine the methylation level of promoter. Wound healing assay and transwell invasion assay were utilized to measure migration and invasion ability of breast cancer cells, respectively.
Results: SP was upregulated while - and were downregulated in breast tumor tissue compared to adjacent normal breast tissues. In addition, we found that - regulated DNMT1 expression in an SP1/SP3-dependent manner, which reduced methylation level of promoter and upregulated expression. SP3 knockdown or - mimic suppressed migration and invasion of MCF-7 and MDA-MB-231 cells whereas overexpression of SP3 compromised miR-506-inhibited migration and invasion.
Conclusions: Our data reveal a novel axis of -/SP3/SP1/DNMT1/ in regulating migration and invasion of breast cancer cell lines, which provide rationales for developing effective therapies to treating metastatic breast cancers.
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| http://dx.doi.org/10.1186/s12935-018-0642-8 | DOI Listing |
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